PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “ascorbic acid”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1978

Use of -l-ascorbic acid, ethocel coated ascorbic acid and ascorbate 2-sulfate in diets for channel catfish, Ictalurus punctatus.

Purified diets with five levels (25, 50, 75, 100, and 200 mg/kg) of supplemental L-ascorbic acid (LAA), and equimolar levels of ethylcellulose coated L-ascorbic acid (EAA) and dipotassium L-ascorbate 2-sulfate dihydrate (AS) were pelleted and fed to 7.9 +/- 0.2 g channel catfish fingerlings for 20 weeks. A dietary level of 23 mg/kg of all three forms of vitamin C prevented spinal abnormalities. Approximately 50 mg/kg diet of either LAA or EAA was sufficient for maximal growth and feed efficiency. Growth response to AS was similar to a Michaelis-Menten type curve and 200 mg/kg diet of AS was necessary to achieve maximal growth. Blood and liver ascorbic acid levels were positively correlated with supplemental levels of LAA, EAA, and AS up to 200 mg/kg; however, blood and liver ascorbic acid levels of fish fed AS were considerably less than those fed LAA and EAA. Weight gains were positively correlated with blood ascorbate levels up to 7 microgram/ml. No measurable level of AS was detected in blood or liver. These results suggest that the rate of enzymatic hydrolysis of AS to LAA or rapid excretion of AS may have been the limiting factor.

Animal Feed↗
PubMed1977

Interaction of erythorbic acid with ascorbic acid catabolism.

There exist altogether four stereoisomers of ascorbic acid. Erythorbic acid (D-isoascorbic acid) differs in the spatial configuration at carbon 5 and has less than 5 per cent of biological vitamin C activity. In guinea pigs, depending on an exogenous supply of ascorbic acid, a possible interaction of erythorbic acid with absorption, transport through the cell membranes at the tissue level, or with catabolism of ascorbic acid has been investigated. After oral administration, results suggest no difference in absorption of these two compounds from the intestine, whereas uptake by the tissues was approximately four to one in favour of ascorbic acid. Feeding experiments with erythorbic acid indicate the availability of ascorbic acid being diminished by 40-60% when administered together with erythorbic acid. Kinetic data on the catabolism of ascorbic acid showed a significant reduction in half-life (50% of the dose excreted) of the vitamin caused by administration of erythorbic acid. The results suggest the oxidative destruction of ascorbic acid in the liver being significantly accelerated. Thus, ingestion of erythorbic acid interacts with newly introduced ascorbic acid by enforcing the breakdown of ascorbic acid. Implications of these findings for the metabolism, availability and nutritional status of ascorbic acid in humans will be discussed.

Animals↗
PubMed1979

[The excretion of hippuric acid and ascorbic acid in the urine of liver-damaged rats (author's transl].

The authors investigated the effects of the administration of thioacetamide, carbon tetrachloride and aminophenazone on the excretion of ascorbic acid and hippuric acid in adult male and female Wistar rats. After a single application of thioacetamide and aminophenazone, the ascorbic acid content in the urine showed a dose-dependent increase, whereas that in the liver had decreased. This increase in the urinary ascorbic acid might be due to a release of stored ascorbic acid from the liver cells. When thioacetamide was given for a prolonged period, the ascorbic acid content in the urine increased at the beginning; later one, at the end of three weeks, it was slightly inferior to the control value. Both single and repeated applications of thioacetamide led to a decrease in the excretion of hippuric acid in the urine, which is attributed to an impairment of the mitochondrial hippuric acid synthesis. Long-term treatment with aminophenazone resulted in an increase of ascorbic acid in the urine, which is indicative of an induction effect, whereas the ascorbic acid content in the liver remained unchanged. There was no effect on the excretion of hippuric acid. In regard to their use in the toxicological evaluation of drugs, these two metabolic effects offer no decisive advantage over current liver function tests.

Aminopyrine↗
PubMed1975

Metabolism of ascorbic acid and ascorbic-2-sulfate in man and the subhuman primate.

Man does not catabolize ascorbate to CO2, whereas the monkey does catabolize ascorbate and ascorbate sulfate to CO2 when these compounds are given orally. However, it takes the same length of time to produce frank scurvy in both man and the monkey, thus indicating that the comparative storage, rate of use, and mode of metabolism of ascorbate is similar in both species. Preliminary feeding and isotope studies conducted on monkeys are in agreement with the fact that only a small amount of labeled ascorbate or ascorbate sulfate equilibrated with body stores. These results are in agreement with published ascorbic acid requirements of 10 mg/kg body weight. In our experiments, 250 mg/day had to be fed to a 10-kg monkey to completely clear all signs of scurvy and return blood ascorbate levels to normal. Ascorbic acid administered intravenously to monkeys appears to equilibrate completely with the ascorbate pool(s). Ascorbate sulfate was found to be a urinary metabolite of both ascorbic-1-14C acid and ascorbic-6-14C acid fed orally to monkeys.

Animals↗
PubMed1979

Effects of ascorbic acid and sodium ascorbate on cyclic nucleotide metabolism in human lymphocytes.

L-ascorbic acid (LAA) augmented cGMP many-fold in highly purified human peripheral blood lymphocytes. The cGMP response occurred within 10 sec and persisted for at least 60 min. D-ascorbic acid (DAA) and dehydroascorbic acid (DHAA) were also equally active in enhancing cGMP concentrations but metabolic precursors of ascorbic acid and other inorganic acids did not increase cGMP levels. Determination of the amount of DHAA contaminating the LAA precluded the possibility that it was solely responsible for the enhanced cGMP levels. The sodium or calcium salts of ascorbic acid did not increase cGMP concentrations. If these neutralized preparations were acidified, increased cGMP concentrations were then noted. In broken cell preparations, LAA, DAA, and DHAA and to a lesser extent sodium ascorbate (NaA) enhanced guanylate cyclase activity while neither inhibited cAMP or cGMP phosphodiesterase (PDE) activity. The possible role of H2O2, fatty acid liberation, prostaglandin production, oxidizing-reducing agents, and free radical formation in mediating the effects of ascorbic acid on cGMP levels were evaluated, but none of these potential mechanisms were definitively proven to be a required intermediary for the cGMP enhancing activity of ascorbic acid. LAA, DHAA or NaA did not induce lymphocyte transformation or modulate lectin-induced mitogenesis.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1977

The effect of ascorbic acid on uric acid excretion with a commentary on the renal handling of ascorbic acid.

Under spontaneous conditions in man and dog, very little ascorbic acid is excreted in urine. Ascorbic acid clearance (C ascorbic acid) is promptly augmented when plasma ascorbic acid is increased by intravenous injection. No net tubular secretion of ascorbic acid is demonstrable in either man or dog when plasma ascorbic acid is elevated to levels as high as 12 mg/100 ml in man, and 28 mg/100 ml in the dog. Nevertheless, both in men and the Dalmatian dog, when the glomerular filtration rate (GFR) is decreased, excreted ascorbic acid in relation to the amount filtered is exaggerated so that C ascorbic acid:GFR approaches unity. It is possible that secreted ascorbic acid is masked under ordinary circumstances, with a more significant contribution of secreted ascorbic acid to total urinary ascorbic acid becoming apparent under conditions of low GFR. In man, when the plasma ascorbic acid level is raised to above 6 mg/100 ml, C urate:GFR rises from control value of 0.081 +/- 0.020, to 0.116 +/- 0.026. In both mongrel and Dalmatian dogs an effect of ascorbic acid on urate excretion is not conclusively shown. The uricosuric effect of ascorbic acid in man may be due to competition with uric acid for renal tubular reabsorptive transport. The difference in the metabolism of ascorbic acid in the dog as compared to man may help account for the inconsistent effect of ascorbic acid on uric acid excretion in the dog.

Aged↗
PubMed1978

Intestinal ascorbic acid transport following diets of high or low ascorbic acid content.

Active transport of ascorbic acid in ileum is mediated by a carrier mechanism at the brush border membrane. This mechanism may show compensatory changes in activity in response to alterations of dietary ascorbic acid content. The unidirectional influx of ascorbic acid across the brush border into epithelial cells of guinea pig ileum was determined in vitro. Influx was significantly reduced in scorbutic animals and following 14 or 28 days of high doses (5 or 25 times normal) of ascorbic acid. The transport rate was reduced by intramuscular administration of ascorbic acid, suggesting that the transport mechanism may respond to circulating levels of the vitamin.

Animals↗
PubMed1977

Effects of chronic vanadium pentoxide administration on L-ascorbic acid metabolism in rats: influence of L-ascorbic acid supplementation.

1. Rats toxicated with vanadium pentoxide showed drastic retardation in growth rate and supplementation of L-ascorbic acid to these rats could not reverse this effect. The urinary excretion of L-ascorbic acid and D-glucuronic acid was decreased in the toxicated group of rats. 2. Considerable lowering of L-ascorbic acid content of the liver tissues of rats was observed under vanadium toxicated conditions. Supplementation of L-ascorbic acid to this group raised the tissue Vitamin C reserve considerably. 3. The normal histological patterns of the liver and kidney tissues of rats were severely disturbed under vanadium toxicated conditions. L-ascorbic acid supplementation to this group of rats showed marked signs of restoration in this respect. 4. Vanadium pentoxide treatment brought about a significant reduction in the biosynthetic capacity of L-ascorbic acid, along with an enhanced utilization of this vitamin. Subsequent supplementation of L-ascorbic acid to the toxicated group of rats was found to be effective in reversing these effects almost to the basal level.

Animals↗
PubMed1977

Ascorbic acid metabolism and the clinical factors which affect tissue saturation with ascorbic acid.

The factors which give rise to tissue desaturation of ascorbic acid are classified and discussed. Nutritional deprivation, normal physiological factors and metabolic factors, and pathophysiological factors may all give rise to acute and continuing ascorbic acid tissue desaturation while the factors continue to operate. Nutritional desaturation can easily be rectified by providing supplementary Vitamin C in adequate dosage. The other factors can only be rectified when the causative mechanism is arrested. Iatrogenic desaturation may be produced by aspirin and several other drugs. While causative factors excluding that of nutrition are operating, it is very difficult if not impossible to restore normal tissue values of ascorbic acid. In consequence side effects which arise from supplementary Vitamin C administration do not arise in these circumstances. The supplementary Vitamin C administration is defined as compensatory administration of Vitamin C. In healthy individuals administration of supplementary Vitamin C can be defined as (large doses). Such large doses may give rise to side effects. The mechanism by which ascorbic acid is involved in the inflammatory response is discussed.

Ascorbic Acid↗
PubMed1977

Effect of PCB (polychlorobiphenyls) on on L-ascorbic acid, pyridoxal phosphate and riboflavin contents in various organs and on hepatic metabolism of L-ascorbic acid in the rat.

Effects of continuous oral administration of PCB (polychlorobiphenyls, 10-100 mg/kg/day, 4 weeks) on tissue levels of L-ascorbic acid (vitamin C), pyridoxal phosphate and riboflavin (vitamin B2) in various organs and on hepatic metabolism of L-ascorbic acid were examined in male Wistar rats weighing 150-250 g. Riboflavin contents in the liver, kidney, brain, heart and testis were not altered by PCB treatments, whereas the hepatic level of pyridoxal phosphate, a biologically active form of vitamin B6, was significantly reduced by PCB administration. Under the same experimental conditions, L-ascorbic acid contents in the liver, kidney, lung and testis showed a significant increase. Histochemical studied revealed that in the adrenal gland, increase of L-ascorbic acid was localized in the fasciculate and reticular zones of cortex, respectively. It was found that increase of L-ascorbic acid in the liver is caused predominantly by activation of biosynthesis at the steps of galactose to D-glucuronic acid and is not due to changes in the catabolic processes of L-ascorbic acid per se. Possible significance of these changes in tissue levels and/or metabolism of vitamins in the occurrence of PCB intoxication is briefly discussed.

Administration, Oral↗
PubMed1975

Ascorbic acid requirements and metabolism in relation to organochlorine pesticides.

Those organochlorine pesticides which possess both high lipoid solubility and high resistance to biodegradation are prone to accumulation in animal tissues and produce relatively long-term effects as toxicants. Such compounds, typified by DDT, Dieldrin, and Lindane, are profound inducers of hepatic microsomal enzymes, including parts of the glucuronic acid and ascorbic acid biosynthetic pathways. Consequently, administering such pesticides to rats in accompanied by enhanced formation and excretion of D-glucuronic acid and L-ascorbic acid, or D-glucaric acid in the case of guinea pigs. Secondarily, the efficiency in biodegrading the pesticides is reduced in ascorbic-acid-deficient guinea pigs with correspondingly greater residue accumulation in tissue. This would aggravate chronic toxic effects of the compounds. Finally, the capacity of the liver to adapt to the presence of such toxicants through enhanced microsomal enzymatic levels appears to be sensitive to its ascorbate status. Impaired enzyme induction is apparent quite early during ascorbic acid depletion in guinea pigs. The enhanced turnover of ascorbate produced by such pesticides, the poor enzymatic adaptation to them during ascorbate depletion and the dependency of the oxidase system upon adequate ascorbate, all point to the central significance of ascorbate status in the liver, and possibly other tissues, as a determinant of their chronic toxicity.

Animals↗
PubMed1979

On the possible involvement of ascorbic acid and copper proteins in leukemia. III. ESR investigations on the interaction between ascorbic acid and some transition metal ions.

The interaction between lyophilized samples of ascorbic acid and Cu2+, Fe3+ or Mn2+ has been investigated by means of ESR spectroscopy. All of the three transition metal ions form complexes with vitamin C, but only in the case of Cu2+ and Fe3+ the interaction results in a reduction of the metal ions. Cu2+ and ascorbic acid seem to form 2 : 1 complexes with an equilibrium constant of about K = 1 X 10(7) mol-1. None of these metal ion complexes exhibits, however, the ESR spectrum obtained with leukemic blood.

Ascorbic Acid↗